Günther, Julia K. and Nikolajevic, Aleksandar and Ebner, Susanne and Troppmair, Jakob and Khalid, Sana
(2020)
Rigosertib-Activated JNK1/2 Eliminate Tumor Cells through p66Shc Activation.
Biology, 9 (5).
p. 99.
ISSN 2079-7737
Abstract
Rigosertib, via reactive oxygen species (ROS), stimulates cJun N-terminal kinases 1/2 (JNK1/2), which inactivate RAS/RAF signaling and thereby inhibit growth and survival of tumor cells. JNK1/2 are not only regulated by ROS—they in turn can also control ROS production. The prooxidant and cell death function of p66Shc requires phosphorylation by JNK1/2. Here, we provide evidence that establishes p66Shc, an oxidoreductase, as a JNK1/2 effector downstream of Rigosertib-induced ROS production, DNA damage, and cell death. This may provide a common pathway for suppression of tumor cell growth by Rigosertib.
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